pathology of respiratory tract infection Flashcards
what 3 factors affect lung infections
microorganism pathogenicity
capacity to resist infection
population at risk
microorganism pathogenicity (3)
primary - very infective and dangerous
facultative - need help to spread e.g. immunosuppression
opportunistic - generally wouldnt be able to cause infection in a healthy person, require significant reduction in defence mechanisms
capacity to resist infection (2)
state of host defence mechanisms
age of patient
population at risk
exposure is necessary to be able to contract the disease
environment - susceptible to host breeding
living conditions and the ability of the pathogen to spread
6 type of URTI
coryza - common cold sore throat syndrome acute laryngotracheobronchitis (croup) laryngitis sinusitis acute epiglottitis
what organism causes the majority of URTI
viral infection
acute epiglottitis causative organism
haemopholius influenzae (type B - Hib) group A beta haemolytic streptococci - complete haemolysis rarely cause by parainfluenza virus type 4 but other viruses may be responsible
what does acute epiglottitis cause
dramatic swelling of the epiglottis
can obstruct the airway
can be fatal in paediatrics but is treatable
3 type of LRTI
bronchitis
bronchiolitis
pneumonia
is bronchiectasis an infection
NO
widening of the airways
build up of XS mucus
prone to infection
what is bronchitis
inflammation of the bronchus
what is bronchiolitis
bronchiole inflammation
caused by RSV (respiratory syncytial virus)
what part of the lung does pneumonia involve
infection involving the conducting part of the lung (alveolar airspace)
4 types of respiratory tract defence mechanisms
MACROPHAGE MICOCILIARY ESCALATOR
general immune system (humoral and cellular)
respiratory tract secretions
URT as a filter
role of upper respiratory tract as a filter
nasal hair acts as a filter
turbulent airflow
lined with mucus to trap material
role of respiratory secretions in preventing infection - problems
XS of secretions e.g. mucus in CF, pulmonary oedema in cardia failure
accumulation of secretions leads to increased chance of infection - acts as a culture medium and organisms can escape the defence mechanisms
3 components of the macrophage mucociliary escalator
alveolar macrophages
mucociliary escalator
cough reflex
role of alveolar macrophages
phagocytic
remove material that has reached the alveolar airspace
role of mucociliary escalator
system of moving mucus from the lower lungs up into the throat
role of the cough reflex
kicks in to help us expel what has been removed from the lungs or we swallow it
is the normal LRT sterile?
YES
what are two important factors that affect the health of the MC escalator
temperature
humidity
viral infection and the MC escalator
viral infections can lead to damage to the MC escalator
e.g. influenza infection: cells are targeted, cytopathic effect, in severe infection the normal ciliated epithelium is replaced by useless virus infected cells, higher risk of 2y bacterial infection
effect of bronchiolitis
bronchioles are usually the target of viral infection
inflammation
inflammatory exudate which accumulates in the airways and can cause respiratory distress
classification of pneumonia (3)
anatomical - what part of the lung is affected
aetiological - circumstances under which the infection occurred
microbiological -appropriate for treatment
aetiological classification of pneumonia
community acquired
hospital acquired (nosocomial)
in the immunocompromised
atypical - unusual organisms
aspiration - substances that should have gone down digestive tract
recurrent - consider how patient’s defence mechanisms are failing
patterns of pneumonia
bronchopnuemonia, segmental, lobar - important for anatomical pneumonia (how much of the lung is infected and where)
hypostatic - lots of lung secretions are accumulating, aspiration, obstructive + retention (both related to cancer), endogenous lipid
bronchopneumonia
affects bronchioles and alveoli surrounding the bronchioles
acute inflammation - neutrophil polymorphs may be seen in sputum sample
focal process - localised infection in the small airways and nearby alveolated lung tissue
often doesnt reach the pleura
usually have another disease which leads to bronchopneumonia e.g. COPD - facultative pathogens
bronchopneumonia on CXR
often bilateral basal patchy opacification
focal nature of consolidation
lobar pneumonia
seen from 1y pathogens in young, healthy people
vigorous inflammtory response and inflammation fills the entire lung/lobe until they can spread out further
outcome/complications of pneumonia
MOST RESOLVE pleurisy, pleural effusion ,empyema - pus accumulates in pleural space organisation lung abscess bronchiectasis potentially fatal
organisation as an outcome of pneumonia
mass lesion - less common, scar/fibrous tissue, often confused with cancer
COP (cryptogenic organising pneumonia - BOOP)
constrictive bronchiolitis
conditions where lung abscesses are more likely to develop
obstructed bronchus (tumour)
aspiration
S. aureus, some pneumococci, Klebsiella
very rare: metastatic in pyaemia, necrotic lung (2y infection)
lung abscess
can be fatal
infection is present as well as destruction and necrosis of the infected tissue - space develops where pus can accumulate
bronchiectasis is the pathological dilation of bronchi due to: (4)
severe infective episode
recurrent infections
proximal bronchial obstruction
lung parenchymal destruction
clinical symptoms of bronchiectasis
75% start in childhood COUGH, ABUNDANT PURULENT FOUL SPUTUM haemoptysis signs of chronic infection coarse crackles clubbing
infections and treatment of bronchiectasis
thin section CT
postural drainage
Abx
surgery - resect affected area f lung
complications of bronchiectasis
acute/chronic suppuration
haemorrhage - severe risk in bronchiectasis, can be fatal
recurrent lung infection
local bronchial obstruction - tumour, foreign body
local pulmonary damage - bronchiectasis
generalised lung disease - CF, COPD
non-respiratory disease, HIV/other, aspiration
aspiration pneumonia
vomiting oesophageal lesion obstetric anaesthesia neuromuscular disorders sedation
where does aspirated material tend to end up
right main bronchus
apical segment of right lower lobe
opportunistic infections
increased change of ‘ordinary infections’
caused by opportunistic pathogens
opportunistic pathogens
not normally capable of producing disease in patients with intact lung defences
low grade bacterial pathogens
CMV
pneumocystitis jirovecii
other fungi and yeasts
normal air flow in airways
bulk flow - laminar (trachea and main bronchi, bronchioles), turbulent (nose)
depends on pressure difference
what causes the blood air barrier
alveolar lung tissue
why is Hb 98% saturated at FIO2 21%
affinity for oxygen
solubility of CO2
very soluble
rapidly equilibrates between blood and air
normal PaO2
10.5-13.5kPa
normal PaCO2
4.8-6.0kPa
type I respiratory failure
PaO2 <8kPa
PaCO2 normal or low
fall in [O2] in peripheral arterial blood
generally occurs as a result of gas exchange failure in part or all of lungs
type II respiratory failure
PaCO2 >6.5kPa
PaO2 usually low
failure to get rid of CO2
failure in ventilation
4 abnormal states associated with hypoxaemia
ventilation/perfusion imbalance
diffusion impairment
alveolar hypoventilation
shunt
pulmonary vascular changes in hypoxia
physiological pulmonary arteriolar vasoconstriction
it is a protective mechanism to avoid sending blood to alveoli short of oxygen
physiological pulmonary arteriolar vasoconstricton
occurs when alveolar oxygen tension falls
can be localised effect
ALL VESSELS CONSTRICT if there is arterial hypoxaemia i.e. global lung disease
why does hypoxaemia occur in pnuemonia
V/Q mismatch - bronchitis/bronchopnuemonia (some ventilation of abnormal alveoli but not enough)
shunt - severe bronchopneumonia, lobar pattern with large areas of consolidation (large amount of lung isn’t engaging in any gas exchange but is still being perfused)
V/Q mismatch
low V/Q is commonest cause of hypoxaemia
low V/Q in some alveoli arises due to local alveolar hypoventilation due to some, focal disease
hypoxaemia due to low V/Q responds well to small increases of FIO2
define shunt
blood passing from R to L side of heart without contacting ventilated alveoli
normally 2-4% shunt
when does pathological shunt occur
AV malformations
congenital heart disease
pulmonary disease
how do large shunts respond to increase in FIO2
they respond poorly
blood leaving NORMAL lung is already 98% saturated
why does hypoxamia occur in COPD (4)
airway obstruction
reduced respiratory drive
loss of alveolar SA
only during acute exacerbation
alveolar hypoventilation
insufficient amount of air moved in and out of lungs
increased PACO2, increased PaCO2
decreased PAO2, decreased PaO2
fall in PaO2 due to hypoventilation is corrected by raising FIO2
why does pulmonary hypertension occur in hypoxic cor pulmonale (5)
PULMONARY VASOCONSTRICTION pulmonary arterioles (muscle hypertrophy and intimal fibrosis) loss of capillary bed 2y polycythaemia (high [RBC] in blood) bronchopulmonary arterial anastamoses
define chronic (hypoxic) cor pulmonale
hypertrophy of the RV resulting from disease affecting the function and/or structure of the lung
except where pulmonary alterations are the result of diseases primarily affecting the L side of the heart or congenital heart disease
